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The **graft-versus-tumor effect** describes the phenomenon whereby donor immune cells—primarily T lymphocytes, but also NK cells—infused during allogeneic hematopoietic stem cell transplantation attack and destroy residual malignant cells in the recipient. This effect is crucial for the curative potential of transplants in hematologic cancers, and its induction relies on recognition of alloantigens and tumor-specific antigens presented by recipient cells. The GvT effect is mechanistically related to—but distinct from—graft-versus-host disease (GVHD); separating antitumor activity from off-target tissue damage remains a central challenge. Molecular studies reveal major contributions from T cell receptor recognition, antigen presentation via MHC/HLA molecules, and effector mechanisms such as cytotoxicity, apoptosis induction, and cytokine release. Clinical enhancement of the GvT effect (e.g., via adoptive NK cell transfer, donor lymphocyte infusion) and control of GVHD are major ongoing research areas. The term is not a molecular target, but a *clinical immunologic effect*. No canonical name, abbreviation, molecular classification, or direct drug interactions as with classic protein targets. Mechanisms centered on donor cell–mediated immunity, apoptosis, and tumor clearance. Principal safety concern is balancing antitumor effect with immune-mediated tissue injury (GVHD).
Donor T cell-mediated cytotoxicity targeting recipient malignant cells via recognition of tumor-specific antigens and alloantigens.\nNatural killer (NK) cell–mediated cytotoxicity.\nActivation of apoptosis pathways in malignant cells via perforin, granzyme, Fas/FasL, and cytokine-mediated mechanisms.
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